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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 93 (1980), S. 293-300 
    ISSN: 0006-291X
    Keywords: [abr] FCS; fetalcalf serum ; [abr] KM; kanamycin ; [abr] PBS^-; phosphate buffered saline ; [abr] PMSF; phenyl methyl sulphonyl fluoride ; [abr] SDS; sodium dodecyl sulfate ; [abr] TPA; 12-0-tetradecanoylphorbol-13-acetate ; [abr] pH 7.4, is composed of 8.0 g NaCl, 0.2 g KCl, 0.2 g KH"2PO"4 and
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 93 (1980), S. 293-300 
    ISSN: 0006-291X
    Keywords: [abr] FCS; fetalcalf serum ; [abr] KM; kanamycin ; [abr] PBS^-; phosphate buffered saline ; [abr] PMSF; phenyl methyl sulphonyl fluoride ; [abr] SDS; sodium dodecyl sulfate ; [abr] TPA; 12-0-tetradecanoylphorbol-13-acetate ; [abr] pH 7.4, is composed of 8.0 g NaCl, 0.2 g KCl, 0.2 g KH"2PO"4 and
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    Location Call Number Expected Availability
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  • 3
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 135 (1988), S. 545-550 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The active metabolite of vitamin D3, 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3), inhibited morphologic and enzymatic expression during differentiation of preadipocyte to adipocyte. In the presence of ∼6.4-20 × 10-10 M 1,25(OH)2D3, the triacylglycerol accumulation was only 50% of that of fully differentiated control cells. High-affinity binding sites for 1,25(OH)2D3 binding component sediments at 3.3 S in 4-24% (w/v) sucrose gradients prepared in hypertonic buffer. Binding assay revealed that Nmax was 70 fmol/mg protein and 90 fmol/mg protein, and Kd value was 170 pM and 37 pM in cell lines ST 13 and 3T3 L1, respectively. We also found that differentiated adipocytes did not contain specific receptors for 1,25(OH)2D3. 1,25(OH)2D3, 1(OH)D3, 24,25(OH)2D3, and 24(OH)D3 all suppressed differentiation of preadipocytes to adipocytes, and the dose required closely reflected the affinities of the various metabolites and the synthetic derivative for 1,25(OH)2D3 receptor. It is suggested that the action of vitamin D3 on preadipocyte differentiation may result from a receptor-mediated event.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 134 (1988), S. 124-130 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: A highly active adipogenic agent was identified in an in vitro adipose conversion system. This agent, ADD 4743 (or ADD), was synthesized by Takeda Chemical Industries (Osaka) as a 3-hydroxy derivative of an oral antidiabetic agent, ciglitazone, and has been presumed to be an active metabolite of the latter substance. When ST 13 mouse preadipose cells were treated with micromolar concentrations of ADD they rapidly and uniformly converted into lipid-accumulating adipocytelike cells within 8-11 days after cell seeding. The degree of adipose conversion and lipid accumulation induced by ADD far exceeded those of the previously known inducing agents such as indomethacin plus insulin. The highly potent adipogenic activity of ADD was confirmed with two other preadipose cell lines (3T3 L1 and RMT rat preadipose cells). In addition to adipogenic activity, ADD inhibited cell proliferation of preadipose cells specifically. Activity of ADD induced lipid accumulation and growth inhibition of ST 13 cells, exhibiting very similar dose-response relationships. Cell proliferation or triacylglycerol content of nonadipocytic mesenchymal cells or epithelial cells were not affected by ADD. These observations strongly suggest that ADD-induced growth inhibition is not due to the nonspecific toxicity of the drug but is tightly associated with the adipocytic character of the treated cells. The present observation provides evidence that ADD would be a powerful agent in studies that involve preadipocyte differentiation.
    Additional Material: 7 Ill.
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  • 5
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 135 (1988), S. 179-188 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Three newly synthesized benzoic acid derivatives (terephthalic acid anilides, chalcone carboxylic acid, and azobenzene carboxylic acid), with a certain structural similarity to retinoic acid, were examined for their retinoid-like bioactivity and their capacity to bind to cellular retinoid binding proteins. Two in vitro systems were used to evaluate their retinoid-like bioactivity: inhibition of adipose conversion of ST 13 murine preadipose cells and growth promotion of murine sarcoma virus (MSV)-transformed 3T3 cells in serum-free culture. All three compounds tested inhibited ST 13 adipose conversion at nanomolar concentrations in a manner similar to classical retinoids such as retinoic acid. The growth-stimulating activity of these compounds on MSV-transformed 3T3 cells was one to two orders of magnitude greater than that of retinoic acid. Simultaneous treatment with these compounds and retinoic acid produced only a barely detectable additive effect, suggesting a common mechanism of action, whereas unrelated mitogens, thrombin, and insulin worked synergistically in combination with retinoic acid. None of the compounds competed with retinol for binding to cellular retinol binding protein. However, two of the three competed with retinoic acid for binding to cellular retinoic acid binding protein. This study provides evidence that the newly synthesized compounds should be included among the retinoids and that their strong biological activity will undoubtedly contribute to the biological and medical application of retinoids.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
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